Streptococcus agalactiae (Group B Strep)

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Streptococcus agalactiae (Group B Strep)

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Glycolysis
Citric acid cycle
Electron transport chain and oxidative phosphorylation
Pentose phosphate pathway
Gluconeogenesis
Anticoagulants: Heparin
Anticoagulants: Warfarin
Anticoagulants: Direct factor inhibitors
Thrombolytics
Antiplatelet medications
Mean, median, and mode
Range, variance, and standard deviation
Standard error of the mean (Central limit theorem)
Normal distribution and z-scores
Paired t-test
Two-sample t-test
Hypothesis testing: One-tailed and two-tailed tests
Correlation
Type I and type II errors
Sensitivity and specificity
Positive and negative predictive value
Test precision and accuracy
Incidence and prevalence
Relative and absolute risk
Odds ratio
Mortality rates and case-fatality
DALY and QALY
Direct standardization
Indirect standardization
Ecologic study
Glycogen metabolism
Physiological changes during exercise
Amino acid metabolism
Nitrogen and urea cycle
Fatty acid synthesis
Fatty acid oxidation
Ketone body metabolism
Cholesterol metabolism
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Lactose intolerance
Cellular structure and function
Cell membrane
Selective permeability of the cell membrane
Extracellular matrix
Cell-cell junctions
Endocytosis and exocytosis
Osmosis
Resting membrane potential
Nernst equation
Cytoskeleton and intracellular motility
Staphylococcus epidermidis
Staphylococcus aureus
Staphylococcus saprophyticus
Streptococcus viridans
Streptococcus pneumoniae
Streptococcus pyogenes (Group A Strep)
Streptococcus agalactiae (Group B Strep)
Enterococcus
Clostridium botulinum (Botulism)
Clostridium perfringens
Clostridium difficile (Pseudomembranous colitis)
Clostridium tetani (Tetanus)
Bacillus cereus (Food poisoning)
Listeria monocytogenes
Corynebacterium diphtheriae (Diphtheria)
Bacillus anthracis (Anthrax)
Nocardia
Escherichia coli
Salmonella (non-typhoidal)
Salmonella typhi (typhoid fever)
Varicella zoster virus
Epstein-Barr virus (Infectious mononucleosis)
Human herpesvirus 8 (Kaposi sarcoma)
Herpes simplex virus
Human herpesvirus 6 (Roseola)
Adenovirus
Parvovirus B19
Human papillomavirus
BK virus (Hemorrhagic cystitis)
JC virus (Progressive multifocal leukoencephalopathy)
Pseudomonas aeruginosa
Enterobacter
Klebsiella pneumoniae
Shigella
Proteus mirabilis
Yersinia enterocolitica
Legionella pneumophila (Legionnaires disease and Pontiac fever)
Serratia marcescens
Bacteroides fragilis
Yersinia pestis (Plague)
Cell signaling pathways
Nuclear structure
DNA structure
Transcription of DNA
Translation of mRNA
Amino acids and protein folding
Nucleotide metabolism
DNA replication
Lac operon
DNA damage and repair
Inflammation
Ischemia
Free radicals and cellular injury
Necrosis and apoptosis
Atrophy, aplasia, and hypoplasia
Metaplasia and dysplasia
Hyperplasia and hypertrophy
Oncogenes and tumor suppressor genes
Cell cycle
Mitosis and meiosis

Transcript

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With Streptococcus agalactiae sometimes called Strep agalactiae, strepto means a chain, coccus means round shape, and agalactiae literally means “no milk”.

So, Strep agalactiae refers to the round bacteria that grow in chains and that was previously known to infect cattle, resulting in reduced milk production.

Later on, Strep agalactiae was found to also be a human potential pathogen responsible for a number of infections that most commonly affect pregnant women and newborns.

Strep agalactiae are also called Group B Strep – GBS - in Lancefield classification developed by an American microbiologist Rebecca Lancefield.

Ok now, a little bit of microbe anatomy and physiology.

Strep agalactiae has a thick peptidoglycan cell wall, which takes in purple dye when Gram stained - so this is a gram-positive bacteria.

It’s non-motile and doesn’t form spores, and also, it’s a facultative anaerobe, meaning that it can survive in both aerobic and anaerobic environments.

Now, a particular trait of Streptococcus species is that they are catalase negative, meaning they do not produce an enzyme called catalase.

This is unlike other common gram positive cocci, like Staphylococcus, which are catalase positive.

When cultivated on a medium called blood agar, Strep agalactiae colonies cause beta hemolysis, also called complete hemolysis.

That’s because Strep agalactiae makes a toxin called beta-hemolysin, that causes complete lysis of the hemoglobin in the red blood cells, making them blood agar change color from red to transparent yellow around the colonies.

However, other Streptococcus species, like Strep pyogenes, are also beta hemolytic.

So to identify Strep agalactiae specifically, the bacitracin test, the hippurate test, or the CAMP test can be done.

With the bacitracin test, a disk of bacitracin is added to the blood agar.

Strep agalactiae is bacitracin resistant, so the colonies remain intact, whereas Strep pyogenes is bacitracin sensitive, so the colonies die off.

With the CAMP test, Strep agalactiae is grown with Staphylococcus aureus on the same blood agar.

Both these bacteria are beta-hemolytic, but Strep agalactiae makes a substance called CAMP factor, which enhances the action of staphylococcal beta-hemolysin.

This results in greater areas of beta-hemolysis where these colonies cross each other on the blood agar plate.

Finally, the hippurate test is based on the fact that Strep agalactiae is the only hippurate positive Strep, because it produces an enzyme called hippuricase or hippurate hydrolase.

To test for this, a colony of bacteria is transferred from the culture to a test tube containing a special hippurate medium, and incubated for two hours. Then, a few drops of a substance called ninhydrin are added to the mix.

With Strep agalactiae, hippuricase converts hippurate to glycine and benzoic acid - and glycine reacts with ninhydrin, making the mix turn deep blue - or positive.

Ok, now, Strep agalactiae has a number of virulence factors, that are like assault weaponry that help it attack and destroy the host cells, and evade the immune system.

First, Strep agalactiae is encapsulated, meaning it’s covered by a polysaccharide layer called a capsule.

The capsule also has pilli, which are hair-like extensions that help the bacteria attach to a host cell.

Additionally, the capsule is rich in sialic acid, which is a substance that can also be found in human cells.

So inexperienced immune cells, like that of a newborn, may confuse Strep agalactiae with self cells, allowing it to survive inside the body.

And finally, Strep agalactiae makes beta-hemolysin, which destroys the host’s tissues and causes hemolysis, meaning it destroys red blood cells.

Key Takeaways

Streptococcus agalactiae, also known as group B streptococcus, is a gram-positive, beta-hemolytic, catalase-negative, and bacitracin-resistant bacterium, which can cause several infections in humans. Most frequently, Streptococcus agalactiae causes neonatal infections like pneumonia, sepsis, meningitis, and septic arthritis. It can also cause chorioamnionitis or cystitis in pregnant females. Treatment involves antibiotics like penicillin G or ampicillin, or Cefazolin and Vancomycin. To prevent Streptococcus agalactiae infections in neonates, intrapartum antibiotic prophylaxis can be administered to vaginally colonized pregnant females.